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Name: Dawn Ortiz
Liver Disease / Pancreatitis Case Study
(Adapted from Clinical Nutrition Case Studies, by Wayne Billon)
Mr. G is a 56 yo construction worker. He is recently divorced with three children in college. He
started drinking heavily when he was in high school and is currently consuming approximately 8
beers and 1-2 shots of whiskey per day. For the last several days, Mr. G has been experiencing
severe epigastric pain with radiation to his back. He has also felt nauseous and has had several
episodes of vomiting. His abdomen is sore to the touch and slightly distended. His temperature
has been elevated. When his symptoms continued for 3 days, Mr. G went to a neighborhood
treatment center to see a physician.
The physician took a medical history and did an examination that included lab values. His labs
were as follows:
Test
Result
Normal
Test
Result
Normal
Na
144 mEq/l
12.0-14.4 sec
ALT
125 u/l
5-40 u/l
K
3.1 mEq/l
3.5-5.3 mEq/l
AST
183 u/l
10-35 u/l
Mg
1.2 mEq/l
1.4-2.5 mg/dl
Total Bili
3.2 mg./dl
0.2-1.3 mg/dl
Cl
103 mEq/l
99-112 mEq/l
Ser. Amylase
685 u/l
5-115 u/l
Glucose
145 mg/dl
70-110 mg/dl
Lipase
463 u/l
7-58 u/l
Serum Albumin
2.9 g/dl
3.5-5.0 g/dl
PT
12.2 sec
135-145 mEq/l
The physician told Mr. G that he had acute pancreatitis with an enlarged liver. Mr. G was told
that his liver enzymes were elevated and that if he continued drinking, he could develop severe
liver disease. The physician wanted to admit Mr. G to the hospital for bowel rest, hydration and
observation, however, Mr. G refused.
The physician told Mr. G that if he stopped drinking, his liver could clear up in a matter of
weeks. Mr. G was encouraged to follow a low fat, high protein diet with absolutely no alcohol,
and call if the pain and discomfort did not clear up within 2-3 days.
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Mr. G's height was 5'11" and he weighed 170 lbs. The physician sent Mr. G home with the
following prescription:
1. Pancreatin (Pancreatin tablets)--enough for 3 days
2. Potassium chloride (Slow-K)--enough for 3 days
The physician advised Mr. G not to take Pancreatin with antacids. He also advised him to take a
multivitamin and mineral supplement daily.
Questions
1. Explain the reasoning behind the diet order Mr. G received: "Low fat, high protein, with
absolutely no alcohol.
A low fat diet is necessary because the liver is responsible for fat conversion and
synthesis. It is also responsible for absorption and storing of fat soluble vitamins,
causing fat toxicity in a damaged liver. The liver is also responsible for detoxifying the
effects of alcohol. A high protein diet is necessary to repair the damaged liver.
2. Outline the instruction you would give Mr. G concerning his diet and liver disease.
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Abstain from alcohol
Consume a high carbohydrate and protein diet with small, frequent meals
Restrict fluid (1000-1500 mL/day) and sodium (< 2 g/day)
25-35 kcal/kg (at least 50% kcal from carbohydrates)
1-1.5 gm/kg protein
Supplement thiamin, folate, Vitamin B12, zinc and vitamin D
3. List the lab values in the chart above that are indicative of liver disease.
Elevated liver enzymes, such as ALT, AST, Bilirubin and Alkaline Phosphatase indicates
build up associated with liver disease. A low PT also indicated slow blood clotting which
is also indicative of liver disease.
4. What abnormal lab values are indicative of pancreatitis?
Elevated amylase and lipase are indicative of pancreatitis, which are digestive enzymes
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secreted by the pancreas.
5. What was the purpose of the physician giving Mr. G the potassium chloride?
Potassium chloride is used to restore potassium levels after prolonged diarrhea and
vomiting. Potassium is important to help sustain blood flow in the body.
6. Give the pathophysiology of fatty liver 2o alcoholism
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Hepatotoxicity, generally reversible in the early stages
Altered NAD/NADH ratio promotes fatty liver through the inhibition of
gluconeogenesis and fatty acid oxidation
Results in the accumulation of triglycerides and fats in the liver cells
Fat cannot be stored and is used preferentially over other energy fuels
Causes disturbances in protein, carbohydrate and lipid metabolism
Mr. G followed his diet and took his medication and began to feel better. He stayed off the
alcohol for 3 or 4 days but then began to have delirium tremens and started to drink again. He
began to have stomach pains different from the epigastric pain he had earlier. He noticed his
abdomen seemed to be becoming distended and he felt like he had no energy.
Mr. G continued to drink heavily. One morning he woke up with severe epigastric pan and
began vomiting blood. Mr. G was brought to the hospital and admitted with GI bleed 2o
esophageal varices, weight gain, ascites, steatorrhea, and alcoholic cirrhosis.
Lab values included
H/H 9.7/27
BUN 35
PT increased
BG 68
ALB 2.4
K 3.0
Na 132
AST, ALT, Alkaline Phosphatase – all increased
Chol 289
TG 310
Ammonia 60
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Mr. TG's weight was now 192 lbs. The physician noted 2+ pitting edema of the lower
extremities. Mr. G was alert and oriented.
Questions continued
7.
Describe the functions of the liver, including from where the blood is supplied and what
is produced by the liver.
The liver is responsible for carbohydrate conversion and storage, protein conversion and
synthesis, fat conversion and synthesis, stores fat soluble vitamins and minerals,
detoxifies drugs and removes nitrogenous wastes (mainly ammonia) and produces bile.
The portal vein carries blood to and from the liver. The liver is responsible for making
glycogen and then converting back to glucose for energy use. The liver synthesizes
many visceral proteins such as albumin, fibrinogen and transferrin. It also oxidizes fatty
acids, produces high density lipoproteins and the active form of vitamin D.
8.
Calculate Mr. G's IBW and percent IBW.
IBW: 75 kg
Mr. G s currently at 116% of his IBW.
9.
Calculate Mr. G’s total energy needs. (Show your calculations and weight basis).
Based on dry weight (UBW) of 77 kg.
Energy: 2310-2695 kcal (30-35 kcal/kg for cirrhosis of the liver patient)
10.
Why is the BUN at 35 mg/dl?
BUN may be elevated due to the esophageal varices and ascites. These conditions cause
excessive plasma protein usually stored in the peritoneal cavity.
11.
Why is blood sugar decreased?
Blood sugar is decreased due to impaired glucose metabolism (impaired glycogenesis,
glyconeogenesis and glycogenolysis). Diet should be high in carbohydrates (50% kcal) to
prevent energy conversion from fat or protein.
12.
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Explain the prolonged prothrombin time.
Due to connective tissue overgrowth, esophageal varices and ascites, blood flow is
disrupted to and from the liver, resulting in prolonged PT. Blood is slowed entering the
liver through the portal vein and leaving the liver through the vena cava.
13.
Why is the cholesterol level elevated?
Altered lipid metabolism and cholesterol synthesis is resulting in elevated LDL
cholesterol build up in the blood.
14.
Why is the serum albumin decreased?
Albumin is synthesized in the liver, therefore serum levels are decreased in a damaged
liver.
15.
List the stages or levels of Hepatic Encephalopathy.
Stage 0: Clinically normal mental status, but minimal changes in memory, concentration
and coordination
Stage 1: Mild confusion, euphoria, or depression, decreased attention; irritability,
disordered sleep pattern
Stage 2: Drowsiness, lethargy, gross deficits in ability to perform mental tasks,
inappropriate behavior, and intermittent disorientation
Stage 3: Somnolent, but can be aroused, unable to perform mental tasks, marked
confusion, present but incomprehensible speech
Stage 4: Coma with or without response to painful stimuli
**Adapted from Haase J. Medical Nutrition Therapy for Liver, Biliary and exocrine
pancreatic disorders, 2004.
16.
What factors may be involved in precipitating Hepatic Encephalopathy?
Hepatic Encephalopathy may be precipitated by GI bleeds, infection, diarrhea and
vomiting.
17.
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What can you expect the ammonia level to be (elevated or low)? How does this affect
your medical nutrition therapy?
Hepatic Encephalopathy is caused by the accumulation of ammonia in the liver that goes
into the blood steam and crosses the blood stream barrier. Ammonia is the byproduct
from the breakdown of protein and is usually converted to urea in a healthy liver.
Therefore, in a damaged liver and in cirrhosis there are elevated levels of circulating
ammonia present.
18.
What are the nutrition-related effects of the following medications, which are often
used to treat these patients?
Neomycin- antibiotic which destroys intestinal bacteria that produce ammonia.
Lactulose- strong laxative used to prevent the absorption of ammonia in the intestine.
These medications are often most effective if used together. GI distress (especially
diarrhea) is a common side effect and therefore result in malabsorption of important
nutrients and deficiency is potassium and magnesium.
19.
How much protein should Mr. G receive per day?
Protein: 92-116 g/day (1.2-1.5 g/kg/day and based on dry weight)
20.
Explain the relationship between alcohol and esophageal varices?
Alcohol abuse causes cirrhosis of the liver which leads to esophageal varices. This is a
non-reversible condition resulting in altered blood flow into the liver, ascites and
edema.
21.
When Mr. G's diet is advanced, what diet modifications would you suggest?
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High calorie (30-35 kcal/kg), high protein diet (1.2 gm/kg)
Moderate-high carbohydrate diet (50% of calories)
Small, frequent meals to optimize daily intake
Focus on nutrient dense foods
Supplement with B complex vitamins, thiamin, folate, and zinc
Avoid alcohol
Avoid excessive fat and fat soluble vitamins
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Reference
Nutrition and Liver/Pancreatic Diseases presentation by: Amanda Gordon, RD, LD, CNSC